Neuroinflammation and Neurodegeneration
September 27 – October 4, 2025
Director: Soyon Hong
UK Dementia Research Institute at University College London
Co-Director: Bart de Strooper
UK Dementia Research Institute at University College London, London, UK & KU Leuven, Belgium
Faculty:
Baljit Khakh, University of California, Los Angeles, USA
Florent Ginhoux, Gustave Roussy Campus, Paris, France
Sonia Garel, École Normale Superieure, Paris, France
Costantino Iadecola, Weill Cornell Medical College, New York, USA
Klaus Nave, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany
Thora Karadottir, Cambridge University, UK
It is becoming increasingly clear that neuroimmune mechanisms critically contribute to neurodegeneration. Neuroglial interactions involving microglia and astrocytes govern proper synaptic function, synchronize clearance of toxic aggregates, and coordinate neuroinflammation. Oligodendrocytes and white matter alterations are observed. Furthermore, emerging data raise a crucial role for peripheral-central immune crosstalk in neurodegeneration. How the different non-neuronal cells contribute to neurodegeneration remains, however, elusive. Therapeutic-wise, there is the grand challenge of balancing the positive and negative consequences of these cellular reactions across ageing and brain borders. Thus, deep insight into how various cells work together to resolve neuroinflammation and mediate neuronal health will be necessary to ultimately change the prognosis of neurodegeneration.
The Faculty will bring leading expertise and insight into neuro-glia-immune mechanisms in neurodegeneration. The Advanced Course will delve into the roles of microglia, astrocytes and OPCs in health and pathology and how brain’s various cell types work together to modulate neuronal function and homeostasis in health (development and adult) and distinct disease states.
Costantino Iadecola
Neuroimmune mechanisms, vascular damage and Alzheimer’s disease
A growing body of evidence suggests that neurovascular damage plays a significant role in Alzheimer’s disease (AD), the leading cause of age-related dementia. This lecture will explore how AD pathology and related risk factors, such as ApoE4 carriage and high blood pressure, impair microvascular function, contributing to cognitive decline. The focus will be on neuroimmune mechanisms, with particular emphasis on the emerging role of border-associated macrophages—brain-resident innate immune cells distinct from microglia—in AD pathology, hypertension, and ApoE4. Finally, the implications of these neurovascular and neuroimmune effects for ARIA syndrome, a treatment-limiting and potentially fatal complication of Aβ immunotherapy, will be discussed.
Bart De Strooper
Amyloid plaques are one of the defining pathologies in Alzheimer’s disease and trigger a long cellular phase which gradually leads to Tau pathology, neuronal dysfunction, granulovacuolar neurodegeneration and necroptosis of neurons. This neurocentric view of the disease is too narrow. Very early on in the disease, a coordinated astro- and microglia response is observed, which actively modulates the disease process. I will explain how this view is gradually taking centre stage in our thinking about this disorder that affects millions worldwide.
Soyon Hong
Microglia are critical contributors to synapse function and health. One important question is how microglia detect and determine which synapses to eliminate and which ones to spare. Emerging data suggest that microglial cell states, including the synapse phagocytosing ones, are influenced not only by changes in neuronal activity but also by surrounding astrocytes and perivascular macrophages. Further, cell-cell crosstalk influencing synaptic fate can also involve adaptive immune signalling along brain borders. I will discuss various potential modulators of microglia-synapse interactions and the consequences of these processes in disease.
Florent Ginhoux
Brain macrophage heterogeneity
Brain macrophages include microglia in the parenchyma, border-associated macrophages in the meningeal-choroid plexus-perivascular space, and monocyte-derived macrophages that infiltrate the brain under various disease conditions. The vast heterogeneity of these cells has been elucidated over the last decade using revolutionary multi-omics technologies. As such, we can now start to define these various macrophage populations according to their ontogeny and diverse functional programs during brain development, homeostasis, and disease pathogenesis. During the lectures, I will first outline the critical roles played by brain macrophages during development and healthy ageing. I will then discuss how brain macrophages might undergo reprogramming and contribute to neurodegenerative disorders, autoimmune diseases, and glioma. Finally, I will speculate about the most recent and ongoing discoveries prompting translational attempts to leverage brain macrophages as prognostic markers or therapeutic targets for diseases that affect the brain.